NEET MDS Lessons
General Pathology
Adrenocortical Hyperfunction (Hyperadrenalism)
Hypercortisolism (Cushing Syndrome) is caused by any condition that produces an elevation in glucocorticoid levels. The causes of this syndrome are
A. Exogenous through administration of exogenous glucocorticoids; the most common causeB. Endogenous
1. Hypothalamic-pituitary diseases causing hypersecretion of ACTH (Cushing disease)
2. Adrenocortical hyperplasia or neoplasia
3. Ectopic ACTH secretion by nonendocrine neoplasms (paraneoplastic)
Pathological features
- The main lesions of Cushing syndrome are found in the pituitary and adrenal glands.
- The most common change in the pituitary, results from high levels of endogenous or exogenous glucocorticoids, is termed Crooke hyaline change. In this condition, the normal granular, basophilic cytoplasm of the ACTH-producing cells in the anterior pituitary is replaced by homogeneous, lightly basophilic material. This is due to accumulation of intermediate keratin filaments in the cytoplasm.
- There is one of four changes in the adrenal glands, which depends on the cause.
1. Cortical atrophy
2. Diffuse hyperplasia
3. Nodular hyperplasia
4. Adenoma, rarely a carcinoma
1. In patients in whom the syndrome results from exogenous glucocorticoids, suppression of endogenous ACTH results in bilateral cortical atrophy, due to a lack of stimulation of the cortex by ACTH. In cases of endogenous hypercortisolism, in contrast, the adrenals either are hyperplastic or contain a cortical neoplasm.
2. In Diffuse hyperplasia the adrenal cortex is diffusely thickened and yellow, as a result of an increase in the size and number of lipid-rich cells in the zonae fasciculata and reticularis.
3. Nodular hyperplasia, which takes the form of bilateral, up to 2.0-cm, yellow nodules scattered throughout the cortex.
4. Primary adrenocortical neoplasms causing Cushing syndrome may be benign or malignant. The adrenocortical adenomas are yellow tumors surrounded by capsules, and most weigh < 30 gm .
Urinary tract infection
Most often caused by gram-negative, rod-shaped bacteria that are normal residents of the enteric tract, especially Escherichia coli.
Clinical manifestations:
frequent urination, dysuria, pyuria (increased PMNs), hematuria, and bacteriuria.
May lead to infection of the urinary bladder (cystitis) or kidney (pyelonephritis).
PARASITIC DISEASES
AMEBIASIS (Entamebiasis)
Infection of the colon with Entamoeba histolytica, which is commonly asymptomatic but may produce clinical manifestations ranging from mild diarrhea to severe dysentery.
Etiology and Pathogenesis
Amebiasis is a protozoan infection of the lower GI tract. E. histolytica exists in two forms: the trophozoite and the cyst.
Two species of Entamoeba are morphologically indistinguishable: E. histolytica is pathogenic and E. dispar harmlessly colonizes the colon. Amebas adhere to and kill colonic epithelial cells and cause dysentery with blood and mucus in the stool. Amebas also secrete proteases that degrade the extracellular matrix and permit invasion into the bowel wall and beyond. Amebas can spread via the portal circulation and cause necrotic liver abscesses.
Symptoms and Signs
Most infected persons are asymptomatic but chronically pass cysts in stools. Symptoms that occur with tissue invasion include intermittent diarrhea and constipation, flatulence, and cramping abdominal pain. There may be tenderness over the liver and ascending colon, and the stools may contain mucus and blood.
Amebic dysentery, common in the tropics but uncommon in temperate climates, is characterized by episodes of frequent (semi)liquid stools that often contain blood, mucus, and live trophozoites.
Chronic infection commonly mimics inflammatory bowel disease and presents as intermittent nondysenteric diarrhea with abdominal pain, mucus, flatulence, and weight loss.
Metastatic disease originates in the colon and can involve any organ, but a liver abscess, usually single and in the right lobe, is the most common
Erythema nodosum is the MCC of inflammation of subcutaneous fat (panniculitis).
- it may be associated with tuberculosis, leprosy, certain drugs (sulfonamides), and is commonly a harbinger of coccidioidomycosis and sarcoidosis.
- commonly presents on the lower extremities with exquisitely tender, raised erythematous plaques and nodules.
- self-limited disease.
Parkinson’s disease
a. Characterized by the degeneration of neurons in the basal ganglia, specifically the substantia nigra and striatum.
b. Histologic findings in affected neurons include Lewy bodies.
c. Clinically, the disease affects involuntary and voluntary movements. Tremors are common. Symptoms include pin-rolling tremors, slowness of movements, muscular rigidity, and shuffling gait.
Clinical genetics (cytogenetics),
This is a method in which inherited chromosomal abnormalities in the germ cells or acquired chromosomal abnormalities in somatic cells are investigated using the techniques of molecular biology.
Cells Of The Exudate
Granulocytes (Neutrophils, eosinophils, and basophils)
Monocytes (and tissue macrophages)
Lymphocytes
Neutrophils (polymorphs).
Characteristics
(1) Cell of acute inflammation.
(2) Actively motile.
(3) Phagocytic.
(4) Respond to chemotactic agents like.
Complement products.
Bacterial products.
Tissue breakdown
Lysosomal enzymes of other polymorphs
Functions
(1) Phagocytosis and intracellular digestion of bacteria.
(2) Exocytosis of lysosomal enzymes to digest dead tissue as the first step in the process of repair.
Eosinophils
Characteristics
(I) Cell of allergjc and immunologic inflammation.
(2) Motile and phagocytic but less so than a neutrophil.
(3) Response to chemotaxis similar to neutrophil. In addition, it is also responsive to antigens and antigen-antibody complexes.
(4) Steroids cause depletion of eosinophils.
Functions
(1) Contain most of the lysosomal enzymes that polymorphs have
(2) control of Histamine release and degradation in inflammation
Basophils (and mast cells)
Characteristics
(1) Contain coarse metachromatic granules.
(2) Contain, histamine and proteolytic enzymes
Functions
Histamine: release which causes some of the changes of inflammation and allergic
reactions. .
Monocytes .
Blood monocytes form a component of. the mononuclear phagocytic system (MPS), the other being tissue macrophages The tissue macrophages may be :
(a) Fixed phagocytic. cells:
- Kuffer cell of liver.
- Sinusoidal lining cells of spleen and lymph nodes.
- Pleural and peritoneal macrophages
- Alveolar macrophages.
- Microglial cells.
(b) Wandering macrophages or tissue histiocytes.
The tissue histiocytes are derived from blood monocytes.
Characteristics
.(1)Seen in inflammation of some duration, as they -outlive polymorphs.
(2) Actively phagocytic and motile.
(3) Fuse readily to from giant cells in certain situations.
Function
(1) Phagocytosis.
(2) Lysosomal enzyme secretion.
(3) Site of synthesis of some components of complement.
(4) Antigen handling and processing before presenting it to the Immune competent cell.
(5) Secretion of lysosyme and interferon.
Giant cells can be
(A) Physiological
Syncytiotrophoblast, megakatyocytes, striated muscle, osteoclast.
(B) Pathological:
Foreign body: in the presence of particulate foreign matter like talc, suture material etc. and in certain infections_e g fungal.
Langhan's type: a variant of foreign body giant cell seen in tuberculosis.
Touton type in lipid rich situations like Xanthomas, lipid granulomas etc.
(iv) Aschoff cell in rheumatic carditis.
(v) Tumour gjant cells e.g. Reid-Sternberg cell in Hodgkin's Lymphoma, giant cells in any malignancy.
Lymphocytes and Plasma cells
These are the small mononuclear cell comprising the immune system
They are less motile than_macrophages and neutrophils and are seen in chronic inflammation and immune based diseases.